There are currently no universally accepted indications and criteria for additional surgical resection of the colorectum after endoscopic resection of the submucosal invasive cancer. The purpose of the present study is to establish accurate indications and criteria for additional surgical resection of the colorectum, based on the prediction of lymph node metastasis, after endoscopic resection of the submucosal invasive cancer. We investigated 140 submucosal invasive colorectal cancers and analyzed the pathologic factors of lymph node metastasis. The tumors were evaluated for pathologic factors in the invasive area of the submucosal carcinoma and were compared between the cases with lymph node metastasis and those without lymph node metastasis. Lymph node metastasis was observed in 13 cases (9%). Univariate logistic regression analysis showed that the depth of invasion, cribriform-type structural atypia, absence of lymphoid infiltration, lymphatic permeation, and venous permeation were statistically significant as risk factors for lymph node metastasis. Multivariate logistic regression analysis showed that the important risk factors included, in decreasing order, lymphatic permeation, absence of lymphoid infiltration, cribriform-type structural atypia, venous permeation, and depth of invasion. Submucosal invasion of 2 mm or more, and/or, depth of lymphatic permeation of 2 mm or more are risk factors for lymph node metastasis. The pathologic criteria based on our results for additional colectomy enables greater accuracy selection of patients who will undergo further surgical treatment after endoscopic resection. Keywords: colorectal cancer; submucosal invasive cancer; criteria for additional colectomy; risk factor of lymph node metastasis Endoscopic resection has become the established standard treatment for mucosal carcinoma and adenoma of the colon. Submucosal invasive cancer may not be diagnosed, in some cases, until after endoscopic resection. Thus, pathologists are increasingly encountering submucosal invasive colorectal carcinomas, which are endoscopically resected. Since 10% or less of cases of submucosal invasive cancer had metastasized to the lymph nodes according to previous reports, 1-7 additional surgical resection of the colorectum after endoscopic resection of submucosal invasive cancer is needed for curative treatment. However, there are currently no universally accepted indications and criteria for additional surgical resection of the colorectum after endoscopic resection of submucosal invasive cancer. As a result, many cases (the remainder, except cases with lymph node metastasis, ie, about 90% of the total cases) involving additional surgical resection of the colorectum constitute overtreatment. Establishment of accurate criteria for additional surgical resection of the colorectum, based on the prediction of lymph node metastasis, after endoscopic resection of submucosal invasive cancer is more than necessary. Thus, toward this goal, we investigated and analyzed the pathologic factors of lymph no...

X-linked ectodermal dysplasia and immunodeficiency (XL-EDA-ID) is an X-linked recessive disease caused by a mutation in the nuclear factor-B (NF-B) essential modulator (NEMO). IntroductionEctodermal dysplasia and immunodeficiency (EDA-ID) is a disease whose clinical features include hypohidrosis, delay of eruption of teeth, coarse hair, and immunodeficiency associated with frequent bacterial infections. [1][2][3][4][5] Two genes responsible for EDA-ID have been identified: nuclear factor-B (NF-B) essential modulator (NEMO; in X-linked-EDA-ID [XL-EDA-ID]) [6][7][8] and IB (in autosomal-dominant EDA-ID). 9 NEMO is necessary for the function of IB kinase, which phosphorylates and degrades IB to activate NF-B. 10 Thus, the defect in NEMO causes various kinds of abnormalities in signal transduction involving NF-B, the interleukin 1 (IL-1) family protein receptors, the Toll-like receptors, vascular endothelial growth factor receptor-3 (VEGFR-3), receptor activator of nuclear factor B (RANK), the ectodysplasin-A receptor, CD40, and the tumor necrosis factor (TNF) receptor. 11 NEMO is also responsible for X-linked-dominant incontinentia pigmenti (IP). 12 Males with IP usually die before birth. The XL-EDA-ID cases reported so far have also been male (with one exception 13 ) but have only one mutated NEMO allele. Residual NEMO activity in XL-EDA-ID and a total lack of NEMO activity in IP can explain the phenotype differences in these 2 populations of males with NEMO defects. 7,8,12 Furthermore, the majority of NEMO mutations in IP patients are large deletions due to recombination, while XL-EDA-ID patients have small mutations such as missense mutations, early stop codons, and stop codon mutations. 12,14 The immunologic features of XL-EDA-ID reported so far consist of dysregulated immunoglobulin synthesis or hyperimmunoglobulin M (hyper-IgM) syndrome, defective antipolysaccharide antibody synthesis (antipneumococcal antibody and isohemagglutinin), reduced lipopolysaccharide (LPS) and IL-1 family protein responses, and defective natural killer (NK) cell activity. 3,4,[6][7][8][15][16][17][18][19] Complete loss of NEMO function is lethal in mice due to liver failure, 20 but studies using conditional knockout mice or recombination-activating gene (RAG) chimera reconstitution have suggested that T and B cells do not develop in the complete absence of NEMO in the mouse. [21][22][23][24] Although XL-EDA-ID is phenotypically different in individuals with different NEMO mutations, there have been no XL-EDA-ID cases reported so far that show a role for NEMO in T-cell development and survival. Now we report a patient with a novel type of XL-EDA-ID whose NEMO expression varied among cell lineages due to reversion mosaicism of a 4.4-kb duplication of a portion of the NEMO gene. The patient provided us with a unique opportunity to elucidate NEMO biology in humans because in this patient we could correlate the NEMO level with cell function in various cell types. In Reprints: Tatsutoshi Nakahata, 54 Shogoin Kawahara-cho, Sakyo, Kyoto 606...

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